inpatient and outpatient care that ismedically necessaryand considered proven.

|go|

A-

Z Index for Clinical Preventive Services

|go|

Epsom–

stheiler A to Z

|go|

Health Line A to Z

|go|



Common OTC Analgesics and

Cough and Cold Medications

|go|



Recommendations for

Clinical Preventive Services

|go|



100 common diseases

|go|

|go|



Springhouse-

Auscultation Skills Breath & Heart Sounds 2ndRev Ed–

2002

|go|

|go|



Μερικα εργαστηριακα

Εχουν γινει τροποποιησεις στις κατευθυντηριες οδηγιες ;

|go|



διαταραχές ύδατος και ηλεκτρολυτών

ηλιαδης φωτης

|go|

Zzzzzz/

Asd/

Pdf maker

|go|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

Cytomegalovirus_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

consult|

|bestPractise|



Ποιους προσβαλλει ο ~ και προκαλει σοβαρη απειλητικηλοιμωξη

:



Χειρουργημενοι γενικως



Καρδιοπαθεις



Τραυματιες



Ανοσοκατεσταλμενοι ????



Ολοι οι παραπανω

Hypergammaglobulinemia_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

consult|

|bestPractise|

Immunoglobulin-Lipoprotein Complex Disorders|go|

Both polyclonal and monoclonal hypergammaglobulinemiasmay cause hypertriglyceridemia.IgG, IgM, and IgA have eachbeen involved. Myeloma, macroglobulinemia, lymphomas, andlymphocytic leukemias have been implicated. Lupuserythematosus and other autoimmune disorders have beenassociated with the polyclonal type. Binding ofheparin

byimmunoglobulin, with resulting inhibition of LPL, can causesevere mixed lipemia.More commonly, the triglyceride-richlipoproteins have an abnormally high density, probably as aresult of bound immunoglobulin, although some may beremnant-like particles. These complexes usually have gammamobility on electrophoresis.

Xanthomatosis associated with immunoglobulin complexdisease includes tuberous and eruptive xanthomas,xanthelasma, and planar xanthomas of large areas of skin. Thelatter are otherwise seen only in patients with cholestasis.Deposits of lipid-rich hyaline material can occur in the laminapropria of the intestine, causing malabsorption and protein-losing enteropathy. Circulating immunoglobulin-lipoproteincomplexes can fix complement, leading tohypocomplementemia. In such patients, administration ofwhole blood or plasma can cause anaphylaxis. Hence, washedred cells oralbumin

are recommended when blood volumereplacement is required.

Treatment is directed at the underlying disorder.Because thecritical temperature of cryoprecipitation of some of thesecomplexes is close to body temperature, plasmapheresisshould be done at a temperature above the criticaltemperature measured in serum

-Globulins are predominately immunoglobulins of theIgG

class.

Increases in-globulins can bemonoclonal, arising from a clonalproliferation of plasma cells or

lymphocytes, orpolyclonal

reflecting aninflammatory response.

Polyclonal-globulins produce abroad-based pattern

in the gammazone, indicating the presence of proteins from many cell lines.

Plasma immunoglobulins are increased either from



acute and chronic inflammatory conditions (polyclonal) or



neoplastic (benign or malignant) expansion of a single clone ofcells (monoclonal).

Increased Polyclonal-Globulins.



Cirrhosis,



myelocytic leukemia,



lupus erythematosus,



RA,



analbuminemia.

Decreased Polyclonal-Globulins.



Nephrotic syndrome,



lymphocytic leukemia,



common variable immunodeficiency,



hypogammaglobulinemia,



protein-losing enteropathies.

The difference between the values for total serumprotein and for serumalbumin

is referred to as theserum globulin fraction of the total serum protein.When the globulin level is increased, fractionationof the globulins is indicated to identify eachcomponent. This is accomplished by serum proteinelectrophoresis (SPEP).



"etiology of Hypergammaglobulinemia "

|google|



In Renal and Perirenal Abscesses

:

hypergammaglobulinemia

in 79%



In Acute Poststreptoccal Glomerulonephritis

:

+

Hypergammaglobulinemia

90%



Hypergammaglobulinemia, which is common in SjÃ¶gren'ssyndrome, has also been associated with RTA

It isunlikely, however, that the development of RTA inSjÃ¶gren's syndrome

issimply due to the associatedhypergammaglobulinemia.



Tubular dysfunction can occur in the absence ofhypergammaglobulinemia, and

is the major catecholamine secreted by the normaladrenal medulla and its secretion is unique to the adrenalmedulla. Epinephrine deficiency is caused by bilateraladrenalectomies, tuberculosis, or hemorrhage.

Epinephrine

is also deficient in patients withcortisol

deficiencyof any cause, because high local concentrations of cortisol inthe adrenal medulla are necessary for transcription of theenzyme

PNMT, which catalyzes the conversion ofnorepinephrine

to epinephrine

in the catecholaminebiosynthetic pathway. Therefore, epinephrine deficiency isfound in patients with secondary hypoadrenalism due topituitaryACTH

withallopurinol, as with uricosuric agents, is begunwith the expectation that it will be continued for years if notforlife.

Allopurinol is often the first urate-lowering drug used. Whenstartingallopurinol,colchicine

or an NSAID should also beused until steady-state serum uric acid is normalized ordecreased to less than 6 mg/dL.

Thereafter colchicine or the NSAID can be stopped, whileallopurinol

is continued.

Aside from gout,allopurinol

is usedas anantiprotozoal

agent(seeChapter 52) and

is indicatedto prevent the massive uricosuriafollowing therapy of blood dyscrasiasthat couldotherwise lead to renal calculi.

Prazosin_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|

adrenergic antagonists_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|

adrenergic alpha-antagonists_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|



Ποιο απο τα παρακατω ειναι αναστολεας των αλφααδρενεργικων υποδοχεων

:



Προπρανολολη



Ατενολολη



Νιφεδιπινη



Κοκκαινη



Πραζοσινη

Osteolysis_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|

Indomethacin_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|



adverse effects of ~ :

|go|



Frequently Used Neurologic Drugs

|go|pdf|

Penicillin_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|



Indications of ~ :

|go|

Drugs of Choice for Suspected or Proved Microbial Pathogens

|go|pdf|

Vincristine_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|



Adverse effects of vincristine

|go|

This drug is used in the treatment of acutelymphoblastic leukemia, lymphomas, and some solidtumors. Its most important toxic side effect, and theone that limits its use as a chemotherapeutic agent, isa peripheral neuropathy. Paresthesias of the feet,hands, or both may occur within a few weeks of thebeginning of treatment; with continued use of thedrug, a progressive symmetrical neuropathy evolves(mainly sensory with reflex loss). Cranial nerves areaffected less frequently, but ptosis and lateral rectus,facial, and vocal cord palsies have been observed.Autonomic nervous system function may also beaffected: constipation and impotence are frequentcomplications; orthostatic hypotension, atonicity ofthe bladder, and adynamic ileus are less frequent. Thepolyneuropathy caused byvincristine

is describedmore fully inChap. 46. Inappropriateantidiuretichormone

secretion and seizures have been reportedbut are uncommon.

Although rarely noted in the literature, the authorshave seen an instance of reversible

posteriorleukoencephalopathy with cortical blindness andheadache after a single dose ofvincristine, identicalto the syndrome reported with the use of calcineurininhibitors (see further on).

The neural complications ofvinblastine

are similar tothose ofvincristine

but are usually avoided becausebone marrow suppression limits the dose of the drugthat can safely be employed.Vinorelbine

is a morerecently introduced semisynthetic vinca alkaloid. Ithas much the same antitumor activity asvincristine

An excess or deficiency ofcalcitoninhas minor effects in humanscompared with the effects

of parathyroid disorders. This patient's hypercalcemia may be due tocoexisting primary

hyperparathyroidism (MEN type

IIa).



Case Discussion: Multiple Endocrine Neoplasia

|go|



Case Discussion: Pheochromocytoma

|go|



Multiple Endocrine Neoplasia, Type 2A

|merck|

=

Sipple's Syndrome



Actions of calcitonin

|go|

The overall importance ofcalcitonin

in the maintenance ofcalcium homeostasis is unclear. Serum calcium concentrationsare normal in patients after thyroidectomy, which removes allfunctioning C cells.



thyroid hormones and catecholamines

|go|

Although plasma catecholamine levels are normal inhyperthyroidism, the cardiovascular effects, tremulousness,and sweating produced by thyroid hormones can be reduced orabolished by sympathectomy. They can also be reduced bydrugs

However, even thoughblockers are weak inhibitors ofextrathyroidal conversion ofT4

to T3, and consequently mayproduce a small fall in plasma T3, they have little effect on theother actions of thyroid hormones. Presumably, the functionalsynergism observed betweencatecholamines

and thyroidhormones, particularly in pathological settings, arises fromtheir overlapping biological functions as well as the ability ofthyroid hormones to increase expression of catecholaminereceptors and the signaling effectors to which they are linked.

Catecholamines_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|

|google|



Mechanism of Action of Selected Small-MoleculeTransmitters

|go|

Calcitonin_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|



Workup of Elevated Calcitonin Overview

|go|

In addition to thyroid cancer, elevated calcitonin levelsmayalso be seen in cancers of

the



lungs,



breast, or



pancreas.



Sometimes levels are elevated in normalpregnant females and in neonates.

If hemorrhagic cystitis develops, the maintenance of a highurine flow may be sufficient supportive care. If conservativemanagement is not effective, irrigation of the bladder with a0.37–0.74% formalin solution for 10 min stops the bleeding inmost cases.N-acetylcysteine

may also be an effectiveirrigant.Prostaglandins (carboprost) can inhibit the process. In extremecases, ligation of the hypogastric arteries, urinary diversion, orcystectomy may be necessary.

emorrhagic cystitis also

occurs in patients who undergo bonemarrow transplantation (BMT). In the BMT setting, early-onsethemorrhagic cystitis is related to drugs in the treatmentregimen (e.g.,cyclophosphamide) and late-onset hemorrhagiccystitis is usually due to the polyoma virus BKV or adenovirustype 11. BKV load in urine alone or in combination with acutegraft-versus-host disease correlate with development ofhemorrhagic cystitis. Viral causes are usually detected by PCR-based diagnostic tests. Treatment of viral hemorrhagic cystitisis largely supportive, with reduction in doses ofimmunosuppressive agents, if possible. No antiviral therapy isapproved, thoughcidofovir

is being tested.



Η αιμορραγικη κυστιτιδα παρατηρειται ως ανεπιθυμητηενεργεια σε ληψη

:



Αζαθειοπρινης



Κορτικοστεροειδων



Χλωραμβουκιλης



Κυκλοσπορινης



Κυκλοφωσφαμιδης



Etiology

|go|

Cystitis_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

|consult|

Hypoparathyroidism_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|

|consult|

Hyperparathyroidism_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e–

medicine|consult|

pseudoprimary aldosteronism_

=liddle'ssyndrome_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

secondary aldosteronism_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

conn adenoma_

= primary aldosteronism

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

Captopril_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

captopril challenge_

|go|

"captopril test "

|google|

="captopril challenge "

|google|

[=for diagnosis of renal artery stenosis

]

"captopril suppression test "

|google|

[=used to assist in the diagnososis ofprimaryaldosteronism

(Conn Syndrome)

]

Inadequacy of captopril challenge test for diagnosing renovascularhypertension in children and adolescents

|go|

The predictive value of the positive test was 43%. In conclusion,we did not find the

CCT, as described for adults, to be of value in children andadolescents



Η δοκιμασια κατοπριλης συμβαλλει σε διαγνωση

:



Δευτεροπαθουςυπεραλδοστερονισμου



Φαιοχρωμοκυτωματος



Ιδιοπαθους υπερτασης



Συνδρομουcushing



Νεφραγγειακης υπερτασης

Επιπλέον

υλικό

: 22/3/2011

"captopril test in secondary hyperaldosteronism"

|google|

Re-evaluation of the captopril test for the diagnosis of primary

|go|

hyperaldosteronism

1.

C. Hambling1,

2.

R. T. Jung1,*,

3.

A. Gunn2,

4.

M. C. K. Browning3,

5.

W. A. Bartlett3

Article first published online: 17MAR 2008

DOI:

10.1111/j.1365-2265.1992.tb02252.x

CONCLUSION

Application of the captopril test to patientsidentified as abnormal by screening confirms allcases of primary hyperaldosteronism but falsepositive or equivocal

results, necessitating further Investigation, mayoccur In some patients with esssentialhypertension

To this end, salt loading is widely used, but thisapproach may be contraindicated in

patients with severe hypertension. The captoprilsuppression test appears as effective as salt loading

in confirming a diagnosis of primary aldosteronism. Inaddition, the captopril test is safe, well

tolerated, and cost-effective

Mosby's Manual

of Diagnosticand Laboratory Tests

plasma renin activity

|go|go|

A determination of the PRA and a measurement of the plasmaaldosterone

level are used in the differential diagnosis ofprimary and secondaryhyperaldosteronism. Patients withprimary hyperaldosteronism (caused by an adrenal tumor thatoverproduces aldosterone) will have an increased aldosteronelevel with decreased renin activity. Conversely, patients withsecondary hyperaldosteronism (caused by certain types ofkidney disease) will have increased levels of renin.

Par 18/3/2011

intravascular volume

_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

extravascular

volume

|////

|

intracellular volume |////

|

gingival hemorrhage_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

Petechiae_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|



Ασθενης με αιμορραγια απο τα ουλα και πετεχειεςστα κατω ακρα–

ποια εξεταση ενδυκνειται κατακυριο λογο

:



Χρονος προνθρομβινης καιinr



Χρονος μερικης θρομβοπλαστινης



Ηπατικα ενζυμα



Ουρια και κρεατινινη ορου



Γενικη αιματος

"gingival hemorrhage Petechiae"

|google|

Το πρωτο που πρεπει να σκεφθουμε ειναιθρομβοκυτταροπενια

human leukocyte antigens_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|//////|

Αιμορραγικες

κενωσεις

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|



Σε ποια απο τις παρακατω κατασταστασεις παρατηρουνται~ :



Αμοιβαδικη δυσεντερια



Εντερικη λοιμωξη απο σιγκελλα



Φλεγμονωδης νοσος του εντερου



Ισχαιμικη κολιτιδα



Ολα τα παραπανω

???????

Risk factors for colonic ischemia

|go|

Shigelladysenteriae / Clinical Findings

|go|

After an incubation period of 1 to 4 days, symptoms beginwith fever and abdominal cramps, followed bydiarrhea,which may be watery at first but later contains bloodand mucus.

The disease varies from mild to severedepending on two major factors: the species ofShigella

andthe age of the patient, with young children and elderlypeople being the most severely affected.Shigelladysenteriae,

which causes the most severe disease, isusually seen in the United States only in travelers returningfrom abroad.Shigella sonnei,

which causes mild disease, isisolated from approximately 75% of all individuals withshigellosis in the United States. The diarrhea frequentlyresolves in 2 or 3 days; in severe cases, antibiotics canshorten the course. Serum agglutinins appear after recoverybut are not protective because the organism does not enterthe blood. The role of intestinal IgA in protection isuncertain.

In contrast to patients with AMI, those with colonic ischemia do notusually appear acutely ill.Bleeding is usually mild, and patientsrarely require blood transfusion.Peritoneal signs, if present, wouldsuggest perforation or peritonitis. Ischemic colitis is usually a singularevent, and only 5% of patients develop a recurrence.

The diagnosis is usually established on the basis of clinical history,physical examination,

and endoscopic or radiologic studies. Althoughmost patients who develop colonic ischemia are elderly, the conditioncan also occur in younger patients. For patients who are younger thanage 50, several precipitants of colonic ischemia should be considered(seeTable 6–2). In young women, the triad of smoking, use of oralcontraceptives, and carriage of the factor V Leiden mutation may beassociated with increased risk of colonic ischemia. Recent reportsindicate that giving penicillin derivatives to patients who harborKlebsiella oxytoca

may precipitate hemorrhagic colitis.

Intestinal Amebiasis

|go|

The most common type of amebic infection is asymptomatic cystpassage. Even in highly endemic areas, most patients harborE. dispar.

Symptomaticamebic colitis

develops 2–6 weeks after the ingestion ofinfectious cysts. A gradual onset of lower abdominal pain and milddiarrhea is followed by malaise, weight loss, and diffuse lower abdominalor back pain. Cecal involvement may mimic acute appendicitis. Patientswith full-blown dysentery may pass 10–12 stools per day. The stoolscontain little fecal materialandconsist mainly of blood and mucus.In contrast to those with bacterial diarrhea, fewer than 40% of patientswith amebic dysentery are febrile.Virtually all patients have heme-positive stools.

Inflammatory Bowel Disease

|go|

IBD is usually diagnosed in older childrenor teenagers, and commonlythe first presentation involves severe acute abdominal pain. In one largeseries, 95% of children <10 years old with Crohn disease presentedinitially with abdominal pain.40

Often, the pain is described as colicky andis associated withdiarrhea, which may be bloody. Abdominal pain isnot the sole presenting symptom, and IBD is associated with fever,weight loss, fatigue, and blood per

rectum.

Clinical Findings

The patient typically complains of abdominal crampsand intermittentbloody diarrhea. A history of previous episodes may be given, and along history of colitis may be present. Weight loss, fever, and anemiamay be present. Cramps may develop gradually or suddenly. Abdominalexamination will vary with etiology and severity of disease. Infectiouscauses (e.g.,Shigella

sp.,Clostridium difficile,Campylobacter

sp.,Entamoeba histolytica) should be systematically ruled out.

mucous membrane_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

|consult|

Epithelium_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

Pem 17/3/2011

Osteocalcin_

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|

cardiovascular mortality

|go|go|FPN++go|ddb|Wikipedia|def1|def2|e

–

medicine|



Associations of total osteocalcin with all-cause and cardiovascularmortality in older men. The Health In Men Study

Currently the most common use for applied genetics inobstetrics and gynecology is in prenatal counseling,screening, and diagnosis. Prenatal diagnosis first came intouse in 1977 with the discovery of the significance of serum-fetoprotein (AFP).

The United Kingdom Collaboration Study found thatelevated AFP in maternal serum drawn between16 and 18 weeks of gestation correlated with anincreased incidence of neural tube defects (NTDs).Since that time, much research effort has been aimed atperfecting the technique. We now can screen not only forNTDs but also for trisomy 21 and trisomy 18. In addition,cystic fibrosis, sickle cell disease, and Huntington's disease,as well as many inborn errors of metabolism and othergenetic disorders, can now be identified prenatally.